Inflammatory arthritis encompasses a diverse group of disorders driven by immune, crystal-induced, or post-infectious inflammation affecting the synovial joints and periarticular structures. While the clinical manifestations often overlap, imaging provides the crucial window into the disease process – allowing visualization of inflammation, tissue damage, and repair across time. Radiology not only refines diagnosis and subclassification but also serves as a biomarker of disease activity and treatment response. Early in the disease course, imaging can detect changes in subclinical disease. Ultrasound (USG) and magnetic resonance imaging (MRI) detect the earliest inflammatory changes – synovial thickening, effusion, hyperemia on power Doppler, and bone marrow edema – before radiographs show structural alteration. MRI, with its exquisite soft-tissue contrast, identifies active osteitis, enthesitis, and pannus formation, predicting erosive progression and guiding timely therapy. USG complements this by offering dynamic real-time assessment, grading vascular activity through European Alliance of Associations for Rheumatology-outcome measures in rheumatology scoring, and directing image-guided interventions. As disease evolves, radiographs remain indispensable for documenting chronic changes such as joint space narrowing, marginal erosions, and ankylosis. Rheumatoid arthritis (RA) typically demonstrates symmetric marginal erosions with uniform joint space loss and periarticular osteopenia, most marked in the small joints of the hands and feet. Psoriatic arthritis shows a unique combination of erosive and proliferative changes, producing “pencil-in-cup” deformities, enthesitis, and asymmetric sacroiliitis. Ankylosing spondylitis – the prototype of axial spondyloarthritis – progresses from subtle sacroiliitis and vertebral “shiny corners” to syndesmophyte formation and complete spinal ankylosis, culminating in the classic “bamboo spine.” Imaging also alerts clinicians to complications such as unstable spinal fractures (carrot-stick fractures) resulting from rigid, osteopenic spines. Crystal-induced arthropathies often pose a diagnostic challenge. Dual-energy computed tomography (CT) now enables specific detection of urate crystals in gout, while USG demonstrates the pathognomonic “double contour” sign. Chondrocalcinosis in calcium pyrophosphate deposition disease and amorphous periarticular calcifications in hydroxyapatite deposition disease are distinct radiographic hallmarks. Recognition of these imaging signatures allows confident differentiation from inflammatory mimics. Quantitative MRI techniques – such as RA MRI score-based semiquantitative scoring, diffusion-weighted imaging, T2 mapping, and dynamic contrast-enhanced MRI – together with microvascular imaging and positron emission tomography/CT, allow earlier detection of inflammatory and metabolic activity. At present, quantitative MRI is used predominantly as a research tool to objectively measure disease activity and treatment response. These approaches may ultimately refine disease monitoring by enabling in vivo quantification of active inflammation and tissue repair. For radiologists, understanding the imaging spectrum across inflammatory arthritis subtypes is fundamental. Correlating imaging findings with clinical and laboratory data sharpens diagnostic precision, guides therapy, and prevents irreversible joint damage. Beyond diagnosis, radiology serves as a longitudinal witness to disease biology – mapping the transition from inflammation to remodeling and helping clinicians achieve treat-to-target control.
Sahu et al. (Mon,) studied this question.